首页> 外文期刊>Addiction biology >Ethanol consumption and pineal melatonin daily profile in rats.
【24h】

Ethanol consumption and pineal melatonin daily profile in rats.

机译:大鼠的乙醇消耗量和松果体褪黑激素的每日分布。

获取原文
获取原文并翻译 | 示例
       

摘要

It is well known that melatonin participates in the regulation of many important physiological functions such as sleep-wakefulness cycle, motor coordination and neural plasticity, and cognition. However, as there are contradictory results regarding the melatonin production diurnal profile under alcohol consumption, the aim of this paper was to study the phenomenology and mechanisms of the putative modifications on the daily profile of melatonin production in rats submitted to chronic alcohol intake. The present results show that rats receiving 10% ethanol in drinking water for 35 days display an altered daily profile of melatonin production, with a phase delay and a reduction in the nocturnal peak. This can be partially explained by a loss of the daily rhythm and the 25% reduction in tryptophan hydroxylase activity and, mainly, by a phase delay in arylalkylamine N-acetyltransferase gene expression and a 70% reduction in its peak activity. Upstream in the melatonin synthesis pathway, the results showed that noradrenergic signaling is impaired as well, with a decrease in beta1 and alpha1 adrenergic receptors' mRNA contents and in vitro sustained loss of noradrenergic-stimulated melatonin production by glands from alcohol-treated rats. Together, these results confirm the alterations in the daily melatonin profile of alcoholic rats and suggest the possible mechanisms for the observed melatonin synthesis modification.
机译:众所周知,褪黑素参与许多重要的生理功能的调节,例如睡眠-清醒周期,运动协调和神经可塑性以及认知。然而,由于在饮酒条件下褪黑激素产生的日变化规律存在矛盾的结果,本文的目的是研究在长期饮酒的大鼠中褪黑激素的每日变化的现象学和推测机制。目前的结果表明,在饮用水中接受10%乙醇的大鼠持续35天的实验表明,其褪黑激素的每日生产量发生了变化,出现了相延迟并减少了夜间睡眠高峰。这可以部分归因于每日节律的丧失和色氨酸羟化酶活性降低25%,主要是芳基烷基胺N-乙酰基转移酶基因表达的相位延迟和其峰值活性降低70%。结果表明,在褪黑激素合成途径的上游,去甲肾上腺素能信号传导也受到损害,β1和α1肾上腺素能受体的mRNA含量降低,并且酒精治疗大鼠的腺体在体外持续丧失了去甲肾上腺素能刺激的褪黑素产生。总之,这些结果证实了酒精性大鼠每日褪黑激素概况的改变,并暗示了观察到的褪黑激素合成修饰的可能机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号